Equine Grass Sickness--Still an Enigma

More than 100 years ago, an outbreak of grass sickness was recognized in Scotland, and this devastating disease remains one of the great unsolved mysteries in equine medicine. We still do not know its cause and, therefore, lack any means for causal therapy; the disease is a continuing threat.

As its name suggests, grass sickness is strongly associated with grazing and occurs in acute, subacute, and chronic forms with a considerable overlap in clinical signs. The major signs relate to partial or complete paralysis of the digestive tract. Considering the nature of the damage to the nervous system, combined with epidemiological factors, a type of toxin is suggested as the causative agent.

Many potential causes have been examined but none has survived scientific scrutiny despite almost 90 years of investigation. The (disease) was associated with exposure to grazing or the ground right from the beginning and therefore it was also considered that grass sickness might be a form of botulism. The first reports of botulism in horses in connection with feedstuffs were reported in the United States and additional cases also were associated with grazing. Beside this, some symptoms of these two diseases are comparable.

That grass sickness might be caused by Clostridium botulinum was first proposed almost 90 years ago in 1923. However, these investigations failed to demonstrate clear evidence and the idea lost favor. Moreover, doubts persisted because of the anaerobic and ubiquitous nature of C. botulinum. In 1999, new interest in the organism began. Researchers showed that green grass blades can contain botulinum toxin. On a European stud where grass sickness occurred twice within eight months, grass and soil samples and necropsy specimens were tested for the presence of bacterial forms and toxin of C. botulinum. Different types of the germ (A-E) and neurotoxin (BoNT) were found and showed that growing grass contained free BoNT. Bacterial forms in soil were numerous in May, but were not found in August and September. It is speculated that biofilms adhere to lower parts of the grass and allow C. botulinum to survive within a bacterial consortium while being trapped and protected from dehydration.

Other indications for the involvement of clostridia are some similarities with the equine atypical myopathy, with Clostridium sordellii as a suspected causative agent. Here, we also encounter a regional, seasonal, and pasture-associated disorder that is characterized by degenerative alterations. Also, environmental factors seem to influence the incidence of both diseases as well as access to pasture, certain weather conditions, and the degree of resistance in older horses. The exact role the toxins of C. sordellii or C. botulinum play in the respective diseases has yet to be defined.

Researchers in 1924 demonstrated statistically highly significant protection against grass sickness by vaccinating horses with a mixture of botulinum toxin and antitoxin, and today work continues in the United Kingdom toward demonstrating efficacy of a botulinum toxoid against equine grass sickness. Such progress will take more time, and we must make sure to use other preventive measures to the best of our knowledge. Careful husbandry and meticulous pasture management must be of the highest standards.

It brings to mind the saying of the French physiologist Claude Bernard (1813-1878): "It is not the germ that causes disease but the terrain in which the germ is found"--an opinion that is older than the grass sickness itself.

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